Diagnostic Cervical Disk Injection

Santhosh A. Thomas

Seth M. Zeidman

There are many causes of neck pain. It is well established that neck pain can be caused by various disorders and diseases that affect the various structures in the neck such as muscles, joints, ligaments, nerves, and disks. Neck pain can present with or without radicular pain into the surrounding structures, but more commonly the radiation is noted into the upper extremities. There is a lack of accord regarding the true causes of neck pain and perhaps even more disagreement exists in the treatment options. Cervical diagnostic disk injection (discography) remains one of the more controversial areas of evaluation of a painful cervical disk believed to be a cause of neck pain. Discography is classically defined as the direct visualization of the intervertebral disk by percutaneous injection of water-soluble iodine solution into the nucleus pulposus with a small-gauge needle. The images are obtained without any additional information to whether the pain is replicated or not. In contrast, provocation discography combines disk stimulation and subsequent morphologic evaluation of the disk via imaging. More than 60 years ago in Scandinavia, Hirsch (1) and Lindblom (2) used direct puncture to study the lumbar intervertebral disk to localize symptomatic levels in patients with low back pain (1). Cervical discography was introduced by Smith and Nichols (3) in 1957 and Cloward (4) in 1958. Later, an analgesic-therapeutic component was incorporated into the radiographic and provocative aspects of the study (5).

Magnetic resonance imaging (MRI) is an excellent study to demonstrate structural abnormalities in the spinal structures, but it cannot identify the source of pain in patients (6, 7 and 8). In the setting of degenerative disks, MRI reveals increased T2-weighted signal within the annulus that often represents annular fissures. MRI remains the initial and many believe it to be the best modality to use in the setting of chronic and acute neck pain. MRI does not distinguish between symptomatic and asymptomatic degenerative disks. Proponents of discography assert that it is the best radiologic method to assess anatomy of the intervertebral disk, especially when used in conjunction with computed tomography (CT) (9,10). Discography can demonstrate abnormalities of the cervical disk not visualized on myelography, plain CT, or MRI. Many experienced clinicians use cervical discography as a diagnostic tool in the evaluation of patients with complex cervical symptomatology (9,11,12). The most important component of the discogram is the use of disk injection for production of pain during injection that accurately reproduces the patient’s symptoms (concordant pain). Opponents of discography argue that although the test may be sensitive, it is nonspecific (13,14). Disks with abnormal appearance can frequently be observed in asymptomatic patients. Opponents further assert that surgical intervention based on diagnostic disk injection is, by its very nature, condemned to limited success.

Despite extensive experience with diagnostic cervical disk injection, the role of discography in evaluation of patients with degenerative cervical disk disease and neck pain remains somewhat controversial and incompletely defined (14,15). This chapter briefly reviews some of the historical background of the procedure; reviews the basic pathophysiology of discogenic pain, technical considerations, and potential complications of discography; and outlines some of the arguments for and against diagnostic cervical disk injection.

HISTORY

Early interest in the anatomy, physiology, and pathoanatomy of the intervertebral disk was fostered by the work of Schmorl (16), who described nucleus pulposus herniation into the vertebral body. Schmorl’s research stimulated additional investigation of the intervertebral disk, the most significant of which was the contribution of Keyes and Compere (17). In the subsequent two decades, there followed an extremely large, diverse literature on disk lesions, notably, disk injury with herniation. Because of the inherent limitations of imaging at the time, the scope of the literature primarily included mechanisms of disk injury, general disk pathology, surgical and nonsurgical treatment of the ruptured disk, and subsequent treatment outcomes.

Aside from a few articles on myelography, relatively little was published before the 1950s regarding the radiographic diagnosis of cervical disk pathology. Lindblom (2) published one of the most significant articles in 1948, reporting the poor sensitivity and specificity of myelography
in demonstrating the herniated disk. This opinion was shared by Scoville et al. (18). Lindblom (2), distressed by the unreliability of myelography, conceived direct puncture to study the intervertebral disk.

In 1957, Smith and Nichols (3) were the first to use diagnostic disk injection, or discography, as a diagnostic tool for evaluation of cervical intervertebral disk degeneration. Diagnostic cervical disk injection technique was subsequently popularized by both Cloward (4,19, 20 and 21) and Smith (22). Working independently, these two investigators developed similar techniques for evaluating chronic discogenic pain. Their premise was based on the observation that injection of a symptomatic disk could reliably produce clinical symptoms and a similar discometric profile. That is, a normal disk accepted a small volume of fluid, and abnormal disks accepted larger fluid volumes. A normal discometric profile was invariably associated with a clinically insignificant, “physiologic” pain response. Additionally, each investigator stressed the relative importance of the concordant pain response on disk distention as opposed to the qualitative appearance of a discogram that was deemed generally nonspecific. In addition, the clinical value of anesthetic disk injection was also evident to both examiners. Ultimately, both Smith (22) and Cloward (4) used diagnostic cervical disk injection technique to facilitate surgical patient selection.

Cloward (4) popularized discography in several articles, advancing the thesis that direct disk puncture provided a greater diagnostic database regarding disk injuries in general and that, as a diagnostic procedure, it was more comprehensive than myelography (4). Furthermore, Cloward wrote that the indications for and chief value of discography were related to its ability to diagnose a discopathic or discogenic basis for a given posttraumatic pain syndrome in the absence of a myelographic defect. Beginning in 1958, Cloward (4) championed discography as a routine diagnostic study. In subsequent years, however, many clinicians began to question the validity of cervical discography as a diagnostic tool.

Holt (23) reported on 50 prisoners at the Missouri state penitentiary who underwent cervical discography without fluoroscopic guidance with large (22-gauge) needles. Injection of sodium diatrizoate produced significant pain in all subjects. Holt (24) concluded that cervical discography was painful, expensive, and without diagnostic value. Cloward (25) and other researchers vehemently refuted the evidence presented by Holt, describing it as scientifically inaccurate and based on false premises and conclusions (26). Many subsequent international researchers reported the validity of cervical discography as a diagnostic procedure. Although his study was fundamentally flawed by improper or at least suboptimal technique, Holt’s work caused the credibility of discography to undergo intense scrutiny.

In 1976, Roth (5) reemphasized the earlier work of Smith regarding the anesthetic injection of the cervical disk. Again using the positive postanesthetic clinical response as surgical selection criteria for discectomy and anterior cervical fusion, Roth reported a high surgical success rate.

Since then, a dramatic polarization of opinion has developed regarding the efficacy of discography. This in many ways reflects the parallel controversy over the efficacy and role of surgery for discogenic pain (15,27).

NONINVASIVE IMAGING AND DISCOGRAPHY

The late 1970s and early 1980s heralded major advances in imaging technology with enhanced sensitivity and specificity for pathoanatomy (28). In conjunction with intrathecal contrast enhancement, CT and MRI revolutionized diagnostic spinal imaging. Computer-based technologies have significantly advanced overall diagnostic capability, but radiographic appearances may be deceiving. It is impossible to predict the clinical relevance of an imaged intervertebral disk lesion accurately. Correlation of symptoms with imaging data is not sufficiently reliable to allow unequivocal determination of the nature, location, and extent of symptomatic pathology. This is particularly true in the patient population with chronic discogenic pain (29).

MRI and CT are recognized as the primary methods for investigation of disk herniation and degeneration. Investigators have contended that discography adds little to the diagnostic workup when CT and MRI are available (13,29). However, retrospective studies describe a generally poor correlation between MRI and provocative discography in the cervical spine (11,30). The ability of MRI to identify and localize the source of cervical discogenic pain accurately has been limited. Because of its invasive nature, discography introduces the risk for infection and neural injury. Many have proposed that MRI could replace the technique and remove the risk for infection.

Parfenchuck and Janssen (31) attempted to correlate the morphology of sagittal T2-weighted MRI of the cervical spine with provocative discography and CT discograms in 52 patients with discogenic pain. They noted a significant correlation between MRI abnormality and pain response to discography. However, the false-positive and false-negative rates were high. MRI was a useful adjunct to cervical discography, but some MRI patterns could not be considered pathologic, and discography was required to diagnose discogenic pain (31,32). Parfenchuck and Janssen (31,32), after comparing the ability of discography, discography with CT, and MRI in detecting a painful disk, concluded that MRI was the only imaging technique with strong correlation. In light of these studies, cervical discography may have a place in assessing patients with chronic severe neck pain with a presumed discogenic pain generator.

Schellhas et al. (33) compared and attempted to correlate MRI and cervical discography in evaluation of patients with discogenic pain. Ten asymptomatic subjects and ten patients with chronic neck pain underwent cervical discography after MRI. Disk morphology and provoked responses were recorded at each level studied. Discographically normal disks were never painful, whereas intensely painful disks all exhibited tears of both the inner and outer aspects of the annulus. Schellhas et al. (33) concluded that MRI was ineffective in detecting significant annular tears and could not reliably identify the source of cervical discogenic pain.

Diagnostic cervical disk injection is an adjunctive diagnostic procedure. High-resolution CT and MRI remain the primary imaging modalities. However, discography may be helpful in delineating symptomatic annular tears and fissures as well as lateral and far-lateral disk herniations, some of which can be missed even on MRI (31). Discography is a reliable means of evaluating the integrity of the intervertebral disk. The normal disk will often accept 0.5 mL of saline or contrast media without difficulty according to Saternus and Bornscheuer (29). Considerable force is required to inject any volume of fluid into a healthy disk, and accommodation of 1 mL or more of liquid by a disk is indicative of either degeneration within the nucleus pulposus or extravasation of material through a rent in the annulus fibrosus. Extravasation of contrast material occurs through fissures and tears of the annulus and may be apparent with both degeneration and herniation.

The type and distribution of pain the injection causes should be noted. Testing the patient’s response to intradiscal injection as well as to intradiscal local anesthetic agent is termed provocation-analgesic discography. Proponents of discography contend that morphologic assessment of the intervertebral disk can be complemented by the critical physiologic induction of pain that is similar or identical to the subjective complaint (concordant pain). The disk or disks that reproduce the patient’s symptoms are the ones that may be amenable to efficacious treatment. Provocation-analgesic discography has been used increasingly in evaluation of patients with chronic discogenic symptoms but is not accepted by many to be of any value.

Recreation of pain with saline or contrast injection in some patients but not in others is troubling, all the more troubling when one is faced with a patient with an asymptomatic but dramatic morphologic derangement. Degenerative patterns are often noted and nonspecific pain often elicited in asymptomatic disks, limiting test usefulness. Concordant pain has been postulated to result from the microenvironment in the intervertebral disk and the sensitized state of annular nociceptors.

DISCOGENIC PATHOLOGY AND INDICATIONS FOR DISCOGRAPHY

Regarding symptomatic cervical disk disorders, the following simple classification encompasses most pathology: (a) symptomatic cervical spondylosis, (b) cervical herniation, and (c) internal disk disruption.

SYMPTOMATIC CERVICAL SPONDYLOSIS

Symptomatic cervical spondylosis has generally been considered a normal aging process. The pathophysiology begins with disk desiccation and progresses to disk space narrowing, marginal osteophytic spurring, and, finally, degenerative changes at the facet joint level. Clinical features vary, yet they correlate to some degree with discal dehydration. Symptoms range from episodic axial neck discomfort to severe acquired spinal stenosis with nerve root or cord entrapment.

CERVICAL HERNIATION

Cervical herniated disk disorders have been well chronicled in modern imaging texts. Sensitivity of MRI for disk prolapse has variably been reported to approach 98%.

INTERNAL DISK DISRUPTION

The final category, internal disk disruption, was initially popularized by Crock (34), who described disk lesions characterized by alteration in internal structure and metabolic functions unassociated with rupture or other definable pathoanatomy. A biochemical basis for deficiency was postulated, a hypothesis subsequently based on certain inflammatory-type pathologic features as shown by microscopy, in addition to intraoperative observations suggestive of peridiscal inflammation. Crock cited the often-observed element of increased peridiscal vascularity with sympathetic trunk matting and softening of the vertebral bodies. Clinical features of internal disk disruption are variable; however, Crock pointed out certain universal features that serve to differentiate the condition from others, such as rupture. A constant symptom described as a deep-seated, dull, aching neck pain was invariable. Shoulder girdle or limb pain was typically described as nondermatomal and generalized, in contrast to the more discrete pain characteristic of nerve root compression. A significant association with headache and constitutional symptoms was also noted.

The cardinal lesion rendering a cervical disk painful is internal disk disruption. The characteristic feature of internal disk disruption is a radial fissure extending to the innervated outer third of the annulus fibrosus. As radial fissures extend to the outer third of the annulus, nerve endings are exposed to the inflammatory and algogenic chemicals produced by nuclear degradation. As a radial fissure develops, fewer and fewer lamellae remain intact to bear the load. At some stage, the threshold for mechanical nociception is attained, especially if the nerve endings have been chemically sensitized. Disk stimulation reveals this condition by showing a reduced threshold for mechanical stimulation of the disk.

Discography has been postulated to provoke pain by either one or some combination of the following mechanisms:

Contrast injection into the disk increases intradiscal pressure. In an abnormal disk, stretching of the annular fibers of the disk stimulates nerve endings.
The injection may result in some biochemical or neurochemical stimulation that causes pain.
The injection may increase pressure at the end plates, or pressure may be transferred to the vertebral body throughout the end plate, resulting in an increase in intravertebral pressure. This theory is supported by studies reporting disk injection resulting in end plate deflection and increased specimen height.
The presence of pain on injection of a seemingly normal disk may be due to transfer of pressure from the injection to an abnormal, symptomatic adjacent disk, thus eliciting a positive pain response.

Pathophysiologic mechanisms evoked include (a) biochemical irritation of adjacent neural structures; (b) spinal
instability resulting in adjacent nerve root irritation; (c) leakage of biochemical antagonist, possibly disk protein metabolite, into the general circulation; and (d) autoimmune reaction through the spinal circulation pathway. Crock (35) advocated discography as the preferable diagnostic method; he believed it to be the only diagnostic tool capable of detecting the condition. Many authors have provided the anatomic and histologic proof required for an intervertebral disk to generate pain (36, 37 and 38). They have shown that the outer one-third to one-half of the annulus is richly innervated with a variety of free and complex nerve endings (16,33,39). Furthermore, Weinstein et al. (38) demonstrated the biochemical means by which a disk can be a pain generator. They demonstrated the presence of substance P, calcitonin gene-related peptide, and vasoactive intestinal polypeptides in the outer one-third of the disk in rats (38). Although the mechanism behind discogenic pain has not yet been proved, there are three proposed hypotheses by which axial pain with and without extremity pain from the disk may occur: mechanical, biochemical, and autoimmune (39,40).

The mechanical model theorizes that the afferent C fibers of the annulus may refer pain both axially and to the extremities. This occurs by the convergence of various primary sensory afferents, serving to innervate differentperipheral sites, on dorsal horn neurons of the spinal cord (41). This convergence signal is then relayed to the cells of the ventrolateral system, crosses over to the ventral white commissure, courses rostrally in the anterolateral funiculus, and supplies inputs to several thalamic nuclei and finally to the somatic sensory areas of the cerebral cortex (42). Therefore, the brain is unable to differentiate the true origin of the signal received from the myriad potential sites that could be feeding into the incoming signal. Consequently, a misperception in the location of the pain may be referred to a relatively distal axial location or the extremities (43).

The biochemical model proposes that biochemical events may lead to intervertebral disk degradation and, ultimately, to inflammation (44,45). Based on the articular cartilage model, it has been theorized that the disk cells themselves are a source of interleukin-1B (IL-1B) (45). IL-1B has been shown to increase dramatically the biosynthesis of matrix metalloproteinases, nitric oxide, IL-6, and prostaglandin E₂ in normal, nondegenerated disks (45). These biochemical agents are thought to inhibit proteoglycan synthesis and induce matrix degradation, resulting in a net loss of proteoglycans within the intervertebral disk. This leads to a dramatic alteration in the biochemical integrity of the disk, culminating in disk degeneration (46). Disk degeneration has been shown to result in the accumulation of elevated concentrations of phospholipase A₂ (PLA₂). PLA₂ is the enzyme responsible for the liberation of arachidonic acid from cell membranes resulting in the production of prostaglandins and leukotrienes at the site of injury. These chemical mediators serve to initiate and propagate the inflammatory cascade.

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